Hemostasis, or the stoppage of blood flow, results from plugging blood flow or from forming a blood clot. Plugging blood flow can be accomplished by exerting pressure on or by sealing the bleeding site. The formation of blood clots results from at least three pathways: (1) by a clot cascade; (2) by rapid constriction of the injured vessel; (3) and by the aggregation of platelets to form a plug on the injured surface of the blood vessel.
The clot cascade pathway is initiated by a series of transformations from inactive zymogens to active proteins. An activated protein, or clotting factor, catalyzes the activation of the next protein. Because the pathway is catalytic in nature, only very small amounts of protein need to be activated in order to activate the clotting process.
Clot cascades are calcium-dependent processes and are induced by either intrinsic or extrinsic means. In the case of induction by intrinsic means, clot formation components present in blood are triggered by contact with an abnormal surface, as compared to normal vascular tissue. In the case of clotting induction by extrinsic means, substances not normally present in blood are added. The clotting cascade can be initiated by denaturing clot proteins, which can be accomplished by the removal of water, including the rapid removal of water; by the addition of heat; or by chemical precipitation.
Clotting cascades, whether induced by intrinsic or extrinsic means, ultimately follow a common pathway. The common pathway includes activating clotting factor X, which then converts prothrombin to thrombin by its proteolytic action. In addition, activation of prothrombin is promoted by the presence of calcium ions and by phospholipid surfaces. Thrombin is responsible for cleaving fibrinogen into fibrin monomers, which results in the formation of a fibrin clot. Fibrinogen is an elongated protein consisting of six polypeptide chains. It is highly soluble in plasma. Upon cleavage of fibrinogen by the proteolytic action of thrombin, four peptide bonds are cleaved, and insoluble fibrin monomers result. Those fibrin monomers spontaneously associate to form fibrin, which takes the form of long, insoluble fibers. Fibrin monomers spontaneously associate to form a fibrin clot because of the removal of negatively charged groups found in fibrinogen. The release of the negatively charged groups by thrombin changes the surface-charge pattern of fibrin monomers, which in turn leads to their aggregation and to hemostasis.
Hemostatic agents control blood loss. Bee's wax is generally known to act as a hemostatic plug and has been used to control bone bleeding. Generally, bee's wax resists hydrostatic pressure and is cohesive. Bee's wax, however, is not resorbable and does not allow bone to grow in the site where it is placed. Therefore, bee's wax is undesirable for controlling blood loss from bleeding bone or in areas associated with bone.
In the field of internal medical care, such as internal surgery, there is a need for controlling bleeding in order to prevent excessive blood loss or hemorrhage. There also is a need to provide a product that can be easily applied to a bleeding site that also can promote both blood clotting and bone growth.